It seems exercise may be able to drastically alter how genes operate, studies show. Genes are not static. They turn on or off depending on the biochemical signals they receive from elsewhere in the body. When turned on, genes express various proteins that in turn prompt a range of physiological actions in the body. It seems exercise may be able to drastically alter how genes operate. One powerful means of affecting gene activity involves a process called methylation, in which methyl groups, a cluster of carbon and hydrogen atoms, attach to the outside of a gene and make it easier or harder for that gene to receive and respond to messages from the body. In this way, the behaviour of the gene is changed, but not the fundamental structure of the gene itself. Remarkably, these methylation patterns can be passed on to offspring – a phenomenon known as epigenetics.
What is particularly fascinating about the methylation process is that it seems to be driven largely by lifestyle. Diet, for instance, notably affects the methylation of genes, and scientists suspect that differing genetic methylation patterns resulting from differing diets may partly determine whether someone develops diabetes or other metabolic diseases.
But the role of physical activity in this has been poorly understood. Groups of scientists recently set out to determine what working out does to the exterior of our genes.
The answer, their recently published results show, is plenty.
Of the studies, perhaps the most tantalising, conducted by researchers affiliated with the Lund University Diabetes Centre in Sweden and published last month in PLOS One, began by recruiting dozens of sedentary but generally healthy adult men and sucking out some of their fat cells. Using new molecular techniques, researchers mapped the methylation patterns on the DNA within those cells. They also measured the men’s body composition, aerobic capacity, waist circumference, blood pressure, cholesterol levels and other markers of health and fitness.
Then, under the guidance of a trainer, the volunteers began attending hour-long spin or aerobics classes about twice a week for six months. By the end of that time, the men had shed fat and inches around their waists, increased their endurance and improved their blood pressure and cholesterol profiles.
Less obviously, they also had altered the methylation pattern of many of the genes in their fat cells. More than 17,900 individual sites on 7663 separate genes in the fat cells now displayed changed methylation patterns.
Other studies have found that exercise has an equally profound effect on DNA methylation within human muscle cells. Scientists from the Karolinska Institute in Stockholm and other institutions took muscle biopsies from a group of sedentary men and women and mapped their muscle cells’ methylation patterns. They then had the volunteers ride stationary bicycles until they had burned about 400 calories. Some rode strenuously, others more easily.
Afterwards, a second muscle biopsy showed DNA methylation patterns in the muscle cells were already changing after that single workout, with some genes gaining methyl groups and some losing them. Several of the genes most altered, as in the fat cell study, are known to produce proteins that affect the body’s metabolism, including the risk for diabetes and obesity.
The implication, says Juleen Zierath, a professor of integrative physiology at the Karolinska Institute and senior author of the study, is that DNA methylation changes are probably ”one of the earliest adaptations to exercise” and drive bodily changes that follow.
The intricacies of that complex process have yet to be fully teased out. Scientists do not know, for instance, whether exercise-induced methylation changes linger if someone becomes sedentary, or if resistance training has similar effects on genes. Nor is it known whether these changes might be passed on from one generation to the next. But it is clear, Ling said, that this is ”additional proof of the robust effect exercise can have on the body” even at a DNA level.
( via theage.com.au )